Postreperfusion

Postreperfusion refers to the period that follows the restoration of blood flow to tissue that has experienced ischemia. While reperfusion is essential to salvage ischemic tissue, it can paradoxically cause additional injury, a phenomenon known as reperfusion injury. The injury results from a burst of reactive oxygen species during reoxygenation, calcium overload, mitochondrial dysfunction, endothelial activation, and inflammatory cell recruitment, which can lead to cell damage or death. Postreperfusion can affect multiple organs, including the heart, brain, liver, and kidney, and is a key consideration in procedures that restore perfusion after ischemia, such as reperfusion therapy for myocardial infarction, thrombolysis or endovascular treatment in stroke, and organ transplantation.

In organ transplantation, postreperfusion syndrome describes immediate hemodynamic instability after graft reperfusion, often with hypotension and metabolic disturbances caused by potassium, hydrogen ions, and inflammatory mediators released by the graft. This syndrome can contribute to early graft dysfunction and systemic inflammatory responses. The severity and clinical impact of postreperfusion injury depend on factors such as the duration of ischemia, the extent of reperfusion injury, and the underlying health of the patient.

Management focuses on supportive care during reperfusion, including careful hemodynamic optimization, correction of electrolyte and acid–base disturbances, and avoidance of additional ischemic stress. Antioxidant and anti-inflammatory strategies have been studied, but definitive, widely adopted pharmacological treatments remain an area of ongoing research. Understanding postreperfusion across organs helps inform strategies to improve outcomes after reperfusion therapies and transplantation.